Oncogenic potential of BEX4 is conferred by Polo-like kinase 1-mediated phosphorylation

Abstract

Cancer: an enabler for defective division Tumors exploit a signaling mechanism that allows them to survive disruptions in cell division that would normally prove lethal. When normal cell division goes awry, it produces cells containing abnormal numbers of chromosomes, which exhibit numerous developmental defects. Researchers led by Geun-Hyoung Ha and Chang-Woo Lee, Sungkyunkwan University School of Medicine, South Korea, have learned how a safeguard that prevents this breaks down in cancer cells. They found that cancer cells produce elevated levels of a protein called BEX4 due to a chemical modification that renders this protein more stable. Cells that experience disrupted chromosomal sorting during cell division normally self-destruct through a process called apoptosis. Excessive BEX4 prevents apoptosis, however, allowing such damaged cells to proliferate. This fuels cancer growth but also creates opportunities for treatment with drugs that inhibit BEX4 stabilization.